Evidence mapPaperPMID 42568465Full record

SynthesisFrontiers in endocrinology2026

Genetic susceptibility to uric acid and selected cardiovascular outcomes: a systematic review and meta-analysis of Mendelian randomization studies.

Chunping Li, Ping Chen, Fangda Zheng

Abstract readSystematic ReviewMeta-Analysis
In one paragraph

Synthesis in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Chunping Li *Department of Cardiology, The Third People's Hospital of Nanning, Nanning, China.
Ping Chen *Department of Pulmonary and Critical Care Medicine, The Fourth People's Hospital of Shenyang of China Medical University, Shenyang, China.
Fangda ZhengDepartment of Laboratory Medicine, The Fourth People's Hospital of Shenyang of China Medical University, Shenyang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Serum urate has been associated with cardiovascular disease in observational studies, but whether genetically predicted higher serum urate levels contribute to specific cardiovascular outcomes remains uncertain. We conducted a systematic review and meta-analysis of Mendelian randomization (MR) studies evaluating serum urate-, hyperuricemia-, or gout-related genetic susceptibility in relation to selected cardiovascular outcomes. Methods: PubMed, Embase, and Web of Science were searched from inception to April 6, 2026. Eligible studies were one-sample or two-sample MR studies assessing relevant urate-related exposures and cardiovascular outcomes. Reporting completeness, overlapping or duplicate estimates, exposure-outcome GWAS sample overlap, and MR-specific risk of bias were assessed before quantitative synthesis. Effect estimates were harmonized and standardized to a 1.5 mg/dL increase in serum urate where applicable. Random-effects inverse-variance meta-analyses, Egger regression tests, leave-one-out analyses, Hartung-Knapp adjusted analyses, and stepwise GWAS-source-restricted sensitivity analyses were performed where applicable. Results: Thirty-two MR studies reporting 105 MR analyses were included. After estimate-level screening and MR-specific risk-of-bias assessment, 26 MR estimates were retained for quantitative synthesis. In primary analyses, genetically predicted higher serum urate was associated with increased risks of coronary heart disease (OR = 1.13, 95% CI: 1.10-1.15), myocardial infarction (OR = 1.13, 95% CI: 1.08-1.17), coronary artery disease (OR = 1.17, 95% CI: 1.08-1.26), atrial fibrillation (OR = 1.07, 95% CI: 1.02-1.12), and heart failure based on IVW estimates (OR = 1.08, 95% CI: 1.05-1.11). However, the atrial fibrillation association did not remain statistically significant after Hartung-Knapp adjustment and was reduced to a single estimate after GWAS-source restriction. In GWAS-source-restricted sensitivity analyses, only myocardial infarction and coronary artery disease retained at least three estimates and remained positively associated with serum urate. Conclusion: Evidence was most consistent for myocardial infarction and coronary artery disease. Findings for coronary heart disease, atrial fibrillation, and heart failure were more limited after stricter source restriction. These results do not establish a broad causal effect on cardiovascular disease as a whole or direct cardiovascular benefit from urate-lowering therapy. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420261380161.

Indexed as

Cardiovascular DiseasesGenetic Predisposition to DiseaseHyperuricemiaUric AcidGenome-Wide Association StudyGoutHumansMendelian Randomization AnalysisUric Acidcardiovascular diseasecoronary heart diseasegoutheart failurehyperuricemiaMendelian randomizationmeta-analysisserum urate

Identifiers

PMID42568465
PMCPMC13447163

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.